The Effects of Deep Brain Stimulation in the Ventral Pallidum and the Central Nucelus of the Amygdala on Food Consumption, Motivation, and Palatability.

Abstract

Deep brain stimulation (DBS) has been shown to be an effective treatment for Parkinson’s disease and other movement disorders including essential tremor and dystonia. Given its success, DBS is also being investigated as a potential treatment for psychiatric disorders including depression, obsessive compulsive disorder, eating disorders, and addiction. Although the specific therapeutic mechanisms of DBS are not known, studies suggest that this type of electrical stimulation may be causing an entrainment or regularization of firing patterns in neurons, interfering with the information being processed in the underlying neural circuit.

The overall goal of this thesis is to evaluate the potential neural interference effects of DBS-like stimulation on motivation and reward consumption. Two structures were targeted: the ventral pallidum (VP), which is thought to be an area of convergence for processing reward and reward-related information, and the central nucleus of the amygdala (CeA), which is thought to be especially involved in focusing motivation for particular cues and rewards. The effects on DBS in the VP and CeA on reward-seeking behaviors, food consumption, and hedonic value of tastes were assessed. Results showed that DBS in the VP produced complex patterns of neuronal firing; however, it did not disrupt neural coding of reward and had only minimal effects on food consumption and motivation. DBS in the CeA also resulted in similar complex firing patterns, and additionally (in contrast to the VP) disrupted neural coding of reward. This disruption was reflected in altered behavior. DBS in the CeA invoked an immediate and profound decrease in the consumption of (p < 0.001) and motivation to work for (p < 0.001) sucrose pellets by more than a factor of four. DBS in the CeA also decreased the hedonic value of and increased aversive reactions to sucrose (p = 0.003).

Overall results suggest the DBS is modulating neural activity in the underlying target structure, but the location of electrode is very important and this DBS-induced change in neuronal firing may or may not disrupt coding for reward. Data suggests that CeA may be an effective target for blocking food consumption and motivation.